The contribution of sleep to hippocampus-dependent memory consolidation.
ABSTRACT There is now compelling evidence that sleep promotes the long-term consolidation of declarative and procedural memories. Behavioral studies suggest that sleep preferentially consolidates explicit aspects of these memories, which during encoding are possibly associated with activation in prefrontal-hippocampal circuitry. Hippocampus-dependent declarative memory benefits particularly from slow-wave sleep (SWS), whereas rapid-eye-movement (REM) sleep seems to benefit procedural aspects of memory. Consolidation of hippocampus-dependent memories relies on a dialog between the neocortex and hippocampus. Crucial features of this dialog are the neuronal reactivation of new memories in the hippocampus during SWS, which stimulates the redistribution of memory representations to neocortical networks; and the neocortical slow (<1Hz) oscillation that synchronizes hippocampal-to-neocortical information transfer to activity in other brain structures.
Full-textDOI: · Available from: Lisa Marshall, Dec 23, 2014
SourceAvailable from: Burkhard Pleger[Show abstract] [Hide abstract]
ABSTRACT: Learning is a complex brain function operating on different time scales, from milliseconds to years, which induces enduring changes in brain dynamics. The brain also undergoes continuous "spontaneous" shifts in states, which, amongst others, are characterized by rhythmic activity of various frequencies. Besides the most obvious distinct modes of waking and sleep, wake-associated brain states comprise modulations of vigilance and attention. Recent findings show that certain brain states, particularly during sleep, are essential for learning and memory consolidation. Oscillatory activity plays a crucial role on several spatial scales, for example in plasticity at a synaptic level or in communication across brain areas. However, the underlying mechanisms and computational rules linking brain states and rhythms to learning, though relevant for our understanding of brain function and therapeutic approaches in brain disease, have not yet been elucidated. Here we review known mechanisms of how brain states mediate and modulate learning by their characteristic rhythmic signatures. To understand the critical interplay between brain states, brain rhythms, and learning processes, a wide range of experimental and theoretical work in animal models and human subjects from the single synapse to the large-scale cortical level needs to be integrated. By discussing results from experiments and theoretical approaches, we illuminate new avenues for utilizing neuronal learning mechanisms in developing tools and therapies, e.g., for stroke patients and to devise memory enhancement strategies for the elderly.Frontiers in Computational Neuroscience 02/2015; 9:1. DOI:10.3389/fncom.2015.00001 · 2.23 Impact Factor
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ABSTRACT: The present study focused on investigating the possible neuroprotective potential of peripheral glibenclamide pretreatment and sleep recovery on sleep deprivation effects in rats and the possible mechanisms of action (s). Adult male rats were sleep deprived for a period of 3 days using grid suspended over water method. Morris water maze was used to reveal the effect of both sleep deprivation and the different treatments on learning and memory. Potential mechanisms were explored applying HPLC-UV determination of hippocampal and cortical monoamines in rats. In addition, blood brain barrier intergrity was determined in different groups using Evans blue dye extravasation method. Sleep deprivation induced learning impairment and learning deterioration and neuromotor deficit. The concentrations of 5-hydroxytryptamine (5-HT), norepinephrine (NE) and dopamine (DA) significantly decreased in both brain cortex and hippocampus after sleep deprivation Moreover, sleep deprivation increased blood brain barrier permeability and induced extravasation of the Evans Blue dye in the tested brain areas. Glibenclamide pretreatment antagonized sleep deprivation-induced learning impairment and learning deterioration, and neuromotor deficit. However, pre-treatments with glibenclamide significantly increased the concentrations of 5-HT and NE in rat cortex and hippocamps and minmized the blood brain barrier permeabilty. Moreover, recovery sleep for 48 hours remarkably antagonized sleep-adverse effects. These changes might suggest that the neurochemical changes and the impairment of blood brain barrier function are-at least partly-the underlying mechanism of adverse effects of sleep deprivation on memory and learning. In addition, the potective and restorative effects of glibenclamide and sleep recovery, respectively, against sleep deprivation might be mediated through rebalance the brain chemistry and restoring the normal function of blood brain barrier.Journal of Global Biosciences 05/2015; 4(4):1971-1981.
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ABSTRACT: During the last decade the what, where and when (WWWhen) episodic-like memory (ELM) task, which is based on the object recognition paradigm, has been utilized for the cognitive phenotyping of mouse mutants and transgenic mouse models of neuropsychiatric diseases. It was also widely used to identify the neuroanatomical, electrophysiological and pharmacological foundations of ELM formation, retention and retrieval. Findings from these studies have helped to increase our understanding of the neurobiology and neuropathology of episodic memory in the context of neurodegenerative and neuropsychiatric diseases. Pharmacological studies identified novel targets that might facilitate episodic memory formation in patients with memory problems. In this review, we attempt to delineate the cognitive operations and processes that might underlie rodent performance in the WWWhen/ELM task. We discuss major issues of the object recognition paradigm, including the problem of familiarity vs. recollection-based object recognition, the problem of novel object-induced neophobia, and propose novel methodological solutions to these issues. In conclusion, the WWWhen/ELM task has proven to be a useful tool in the fields of behavioral and translational clinical neuroscience and has the potential to be further refined to address major problems in animal memory research. Copyright © 2015. Published by Elsevier Ltd.Progress in Neurobiology 04/2015; DOI:10.1016/j.pneurobio.2015.04.002 · 10.30 Impact Factor